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Biomedical subjects

P G Gibson

Publications and source records attributed to P G Gibson.

At least 19 recordsLinked to original sources

Chemotherapy for malignancy induces a remission in asthma symptoms and airway inflammation but not airway hyperresponsiveness.

Inflammation with infiltrations of eosinophils and mast cells into the walls of airways is considered to increase airway hyperresponsiveness (AHR), which in turn characterizes asthma. We present a child with AHR in whom the clinical course of asthma was related to eosinophilic bronchitis. Our patient was admitted at age 6 months with bronchiolitis and at age 4 years with asthma. Inhaled corticosteroids were begun at age 7 years. At age 8 he developed a meningeal sarcoma. While on chemotherapy, his asthma symptoms resolved and he no longer required prophylactic asthma treatment. After 14 months off all chemotherapy, he again had mild episodic asthma. While receiving chemotherapy for malignancy, he had an admission with a coagulase negative staphylococcal bacteremia. During sputum induction with 4.5% saline, he developed cough, wheeze, and a 20% reduction in peak expiratory flow (220 to 180 L/min) that reversed after treatment with salbutamol. The sputum cell count was 1.7 x 10(6)/ml with 1.1 x 10(6) being neutrophils. Two weeks later and prior to the induction of the second sputum, a 21% increase in FEV1 was recorded after bronchodilator inhalation (82% to 99% of predicted). The second sputum contained 2.7 x 10(6)/ml cells with 1.6 x 10(6)/ml neutrophils. Neither eosinophils nor mast cells were identified in the sputum. A third sputum obtained 14 months after the cessation of chemotherapy showed a sputum cell count of 16 x 10(6)/ml, with 11.6 x 10(6) neutrophils and 0.4 x 10(6) eosinophils; no mast cells were detected. A reversible 15% reduction in FEV1 was detected on hypertonic saline challenge testing. This boy had persistent airway hyperreactivity and reversible airways obstruction on three occasions during and following chemotherapy. When he developed asthma symptoms, his sputum contained neutrophils and eosinophils; while on chemotherapy his sputum did not contain eosinophils and he was symptom-free and off all asthma therapy. One can speculate that chemotherapy for malignancy can induce a remission in asthma symptoms but not AHR, and remission in symptoms is associated with a lack of eosinophilic or mast cell infiltrates in the sputum.

Asthma

Airway inflammation after treatment with aerosolized deoxyribonuclease in cystic fibrosis.

Recombinant human deoxyribonuclease (rhDNase) has been shown to reduce sputum viscoelasticity and to improve lung function in patients with cystic fibrosis (CF). The aim of this study was to determine whether airway inflammation would decrease after administration of rhDNase. Twenty patients with CF and chronic suppurative lung disease inhaled 2.5 mg of rhDNase daily for 1 month. Before and after the 1-month trial, lung function was measured and sputum was obtained, either after spontaneous expectoration or after sputum induction with hypertonic saline. Sputum total cell and differential counts were measured using techniques previously described. The mean age of the patients was 16.8 years (range, 6.7-27.5). After 1 month of rhDNase, mean FEV1 increased from a baseline of 62.3% predicted to 70.8% (P= 0.02, paired t test); and FVC increased from 74.4% to 83.9% predicted (P=0.007). No significant differences were found in sputum cytology before or after rhDNase (median total cell counts 16.0 x 10(6)/ml vs. 19.3 x 10(6)/ml, P=0.68). Thirteen patients had a 10% or greater increase in FEV1 after rhDNase (responders). Initial lung function was less in responders than in nonresponders (53.5% vs. 78.6%, P=0.007). There was no significant change in total cell count and neutrophil count after rhDNase in either responders or nonresponders. We conclude that airway inflammation, as measured by total cell counts in sputum, was a prominent feature in cystic fibrosis, and neutrophils were the dominant inflammatory cells. Although the administration of rhDNase resulted in significant improvements in FEV1, there was no evidence of accompanying changes in airway inflammation.

Administration, Inhalation

Use of induced sputum to examine airway inflammation in childhood asthma.

Airway inflammation is important in the pathogenesis of asthma, during which it may lead to symptomatic exacerbations and increases in asthma severity, as well as contribute to future decline in asthma status. The use of induced sputum has emerged as an important and useful technique to study airway inflammation. It has particular advantages in the study of childhood asthma because it is noninvasive and allows samples to be collected on repeated occasions in children over 7 years of age. The results of cell counts are reliable when the sputum is processed in a standardized manner involving selection from saliva, cell dispersion, and quantitative cytology. Children with asthma have increased eosinophils and mast cells, which may persist even with high doses of inhaled corticosteroid therapy. During a severe exacerbation of asthma, there is an intense and heterogeneous inflammatory response involving eosinophil and neutrophil accumulation and activation. Characterization of the relevance of airway inflammation in children with asthma is important.

Asthma

Chronic cough resembles asthma with IL-5 and granulocyte-macrophage colony-stimulating factor gene expression in bronchoalveolar cells.

BACKGROUND: Chronic cough is a multifactorial condition, which, like asthma, can be associated with eosinophilic airway inflammation. In asthma, airway eosinophilia is believed to be mediated by cytokines such as interleukin-5 and granulocyte-macrophage colony stimulating factor (GM-CSF). The role of these cytokines in chronic cough is unclear. OBJECTIVE: The aim of this study was to examine gene expression for IL-5 and GM-CSF in chronic cough and compare the results with those found in asthma. METHODS: We studied adults with asthma (n = 12), chronic cough responsive to inhaled corticosteroid (ICS-responsive cough) (n = 9), and chronic cough not responsive to inhaled corticosteroid (non-ICS-responsive cough) (n = 4). Bronchoalveolar lavage (BAL) was performed, and cytokine gene expression was assessed by using a semiquantitative reverse transcriptase polymerase chain reaction. RESULTS: IL-5 mRNA was expressed by BAL cells from nine of 12 asthmatic subjects and six of nine subjects with ICS-responsive chronic cough. IL-5 mRNA was not detected in subjects with non-ICS-responsive chronic cough (zero of four subjects, p < 0.05). GM-CSF mRNA was expressed in BAL cells from seven of 12 asthmatic subjects and six of nine subjects with ICS-responsive cough. GM-CSF mRNA was not detected in non-ICS responsive cough subjects (zero of four subjects, p < 0.05). GM-CSF gene expression was related to the degree of methacholine airway responsiveness in asthmatic subjects (r = -0.59). CONCLUSION: We conclude that chronic cough, like asthma, is associated with airway inflammation and gene expression for IL-5 and GM-CSF. Ongoing expression of these cytokines is likely to be related to the persistence of airway inflammation and chronic cough.

Administration, Inhalation

Peer-led asthma education for adolescents: impact evaluation.

PURPOSE: To examine the impact of a peer-led asthma education program on asthma knowledge, attitudes, and quality of life among adolescents. METHODS: A controlled trial was conducted in two girls' high schools situated in an area of high unemployment and low socioeconomic status, and with a large non-English-speaking community. One school received the intervention and the second school acted as a comparison school. The Triple A (Adolescent Asthma Action) program was implemented in the intervention school and involved Year 11 student peer leaders instructing Year 10 students about asthma. The Year 10 students then developed asthma-related health messages into student asthma performances which were presented to the main student body. Outcomes were evaluated by questionnaire. RESULTS: The Triple A program led to a significant improvement in asthma knowledge in both students with asthma and their peers. This effect occurred not only in students conducting the asthma performances (Year 10), but also in students in the audience (Year 7). Students held favorable attitudes toward asthma, with high degrees of tolerance and moderate internal locus of control. Asthma-related quality of life was not altered by the intervention. CONCLUSION: Peer-led asthma education was well received in the high school setting and led to important improvements in asthma knowledge among students with asthma and their peers.

Adolescent

Induced sputum eosinophil cationic protein (ECP) measurement in asthma and chronic obstructive airway disease (COAD)

BACKGROUND: Induced sputum is a useful way to monitor airway inflammation in asthma, but cell counts are time-consuming and labour intensive. OBJECTIVE: The aim of this study was to evaluate a novel processing method using eosinophil cationic protein (ECP) as a biochemical marker of sputum eosinophil number and activation in subjects with asthma and other airway diseases. METHODS: Sputum was dispersed with dithiothreitol and centrifuged to yield cell free supernatant and a cell pellet. The pellet was treated with a cellular lysis buffer to release cell-associated ECP. ECP was measured in sputum supernatant and in the lysed cell pellet and was compared with sputum eosinophil counts in 31 adults with asthma, chronic obstructive airway disease (COAD), bronchiectasis and healthy controls. The ratio of supernatant to pellet ECP was evaluated as an index of eosinophil degranulation. The effect of sputum processing reagents and storage time on ECP measurement was also evaluated. RESULTS: ECP measured in the cell pellet lysate correlated closely with sputum absolute eosinophil counts across a range of subject groups (r = 0.72, P = 0.004). Sputum eosinophil counts were less well correlated with supernatant ECP levels (r = 0.54, P < 0.05). Incubation with dithiothreitol or lysis buffer did not influence ECP measurement and sputum ECP levels were stable over a 6-9 month period. Sputum supernatant and pellet lysate ECP concentrations were increased in stable asthma, asthma exacerbations and COAD/bronchiectasis (P < 0.05). The ratio of supernatant to pellet ECP was used as an index of eosinophil degranulation and found to be elevated in asthma exacerbations, COAD and bronchiectasis, but not in stable asthma. CONCLUSION: The measurement of ECP in the sputum cell pellet provides a reliable and efficient estimate of sputum eosinophil counts which can potentially be used in clinical trials and epidemiological surveys. The ECP ratio may be a useful marker of eosinophil activation, and was increased in asthma exacerbation and COAD. The increased ECP in COAD reflects a non-selective accumulation of eosinophils in this condition.

Adult

Epidemiological association of airway inflammation with asthma symptoms and airway hyperresponsiveness in childhood.

The role of airway inflammation in childhood asthma is not well defined, despite modern treatment approaches recommending potent anti-inflammatory therapy for an increasing number of children. In this study, induced sputum analysis was used to investigate the relationships among sputum inflammatory cells (eosinophils and mast cells), asthma symptoms, and airway hyperresponsiveness to hypertonic saline in a cohort of 170 children aged 8-14 years. Children who reported asthma symptoms in the past 2 wk had a 2. 25-fold (95% to CI, 1.20-4.24) increased odds of having significant sputum eosinophilia. Hyperresponsiveness to hypertonic saline was strongly associated with higher levels of sputum eosinophils ([OR] 4. 36, 1.70-11.20), sputum mast cells (OR 7.46, 2.48-22.75), and nasal eosinophils (OR 4.73, 1.89-11.86). Interestingly, boys were more likely than girls to have features of airway inflammation (sputum mast cells, OR 3.33, 1.15-9.65; nasal eosinophils, OR 3.25, 1.72-5. 97), which is consistent with the known increase in asthma prevalence in boys in this age group. Airway inflammation with eosinophils and mast cells is likely to be important in the pathogenesis of asthma in childhood. Induced sputum analysis can be used to evaluate this problem and has the potential to be a useful tool for monitoring therapy.

Adolescent

Persistence of sputum eosinophilia in children with controlled asthma when compared with healthy children.

We aimed to describe induced sputum cell counts in healthy nonasthmatic children, and to compare these to children with controlled and uncontrolled asthma. Following clinical assessment and spirometry, ultrasonically nebulized hypertonic saline was used to induce sputum from children with asthma (n=50) and without asthma (n=72). Sputum was dispersed and cell counts performed to yield total and differential cell counts. Specific stains were used for eosinophil and mast cell counts. All of the children with asthma were receiving inhaled and/or oral corticosteroids. Current asthma control was assessed in terms of symptoms and lung function. Children were classified as controlled on inhaled corticosteroids (no current symptoms, normal lung function n=15), current symptomatic asthma (n=16) and asthma exacerbation (n=11). It was found that eosinophils comprised a median 0.3% (interquartile range (IQR): 0, 1.05) of cells in sputum from healthy children. Sputum eosinophils (4.3% (IQR: 15, 14.1) p=0.0005) and epithelial cells (14% (IQR: 6, 19.4) p=0.0005) were significantly higher in children with asthma than in nonasthmatic children. Children whose asthma was controlled, as well as those with symptoms, had more sputum eosinophils and epithelial cells than the nonasthmatics. Mast cells were found in the sputum of only four of the 42 children with asthma. This study demonstrates that eosinophilic airway inflammation and epithelial damage can occur in children with asthma. Airway inflammation persists even in those children who are receiving inhaled corticosteroids, have normal lung function and good symptomatic control of their disease.

Administration, Inhalation

Severe exacerbation of chronic obstructive airways disease: health resource use in general practice and hospital.

The objective of this study is to examine the treatment of exacerbations of chronic obstructive airways disease (COAD) in the hospital and in the community setting using a retrospective study of patients admitted to a major teaching hospital combined with a general practice chart audit. The admission records for 248 admissions from 128 patients were reviewed. Most patients (70%) had visited their GP within 2 weeks of admission, antibiotics were prescribed for 30% of the exacerbations while 51% were treated with ingested corticosteroids. During hospitalization, features of infection were present in 64% (n = 159) of exacerbations and 79% (n = 196) received antibiotics. Patients were also treated with nebulized bronchodilators, oxygen and corticosteroids (82%). The median length of stay was 10 days (range 0-55). There was a high readmission rate (70%) at 1 year for exacerbation of COAD during the study period. Exacerbations of COAD frequently demonstrated the clinical features of infection. Treatment in general practice was less intensive than in hospital, and there is a need to reconcile these differences with studies of early therapy with antibiotics and corticosteroids. Although corticosteroids were used less often in general practice, the literature in this area is not conclusive and the evidence supporting guideline recommendations is not explicit. There are opportunities to examine the role of early therapy and early discharge programmes to minimize the cost burden from exacerbations of COAD.

Adrenal Cortex Hormones

CD36 forms covalently associated dimers and multimers in platelets and transfected COS-7 cells.

CD36 is a transmembrane glycoprotein expressed on the surface of a number of cell types. The analysis of CD36 from platelets using immunoblotting, gel filtration, and native PAGE indicated the presence of high molecular complexes exceeding the Mr of monomeric CD36. Experiments using transfected COS-7 cells revealed these complexes were homodimers and -multimers of CD36. The multimers could be dissociated by treatment with a reducing agent, indicating they were formed by intermolecular cysteine-bridging. Mutagenesis of the cDNA for CD36 implicated the cysteines in the extracellular domain of the molecule. The potential physiological roles of CD36 multimerisation are discussed.

Animals

A systematic evaluation of mechanisms in chronic cough.

We tested the hypothesis that hyperresponsiveness of the upper airway (UAHR) is present in patients with chronic cough of diverse etiology. We determined the frequency of bronchial hyperresponsiveness (BHR), hyperresponsiveness of the upper airway, sputum eosinophilia, pulmonary aspiration, and psychological symptoms in adults with chronic cough. Consecutive adults (n = 30) presenting to a tertiary referral clinic with chronic cough were compared with a group of 20 asymptomatic adults. Measurements included histamine provocation testing with measurement of flow volume curves to determine inspiratory and expiratory airflow obstruction; hypertonic saline induced sputum for analysis of eosinophils, mast cells and lipid-laden macrophages; and a validated psychological symptom questionnaire. Symptomatic rhinitis and gastroesophageal reflux were common causes of chronic cough. BHR occurred in seven patients (23%) and in no control subjects (p < 0.05). UAHR occurred in 40% of patients with cough and in four (20%) control subjects (p > 0.05). Eosinophils were present in the sputum of more patients with cough than control subjects (50% versus 19%; p < 0.05). High degrees of eosinophilia were present in six patients with cough, including three without BHR. No subject had significant lipid-laden macrophages. There was greater somatization in patients with chronic cough; ten subjects scored in the clinically significant range (p < 0.05). Abnormalities in one or more of these tests were 7.67-fold (95% CI 1.83-34.52) more likely to occur in cough patients than control subjects. We conclude that chronic cough is a nonspecific symptom that is associated with several apparently unrelated mechanisms. These include UAHR, somatization, BHR, and eosinophilic bronchitis. UAHR cannot be implicated as a single unifying mechanism. These findings emphasize the need to systematically evaluate several different causes of cough in patients who present with chronic cough.

Adult

Nasal inflammation and chronic ear disease in Australian Aboriginal children.

OBJECTIVE: Chronic middle ear disease is common in Aboriginal children, and may be linked to nasal inflammation and Eustachian tube dysfunction. The pattern of nasal inflammation is unknown. The study reported here was performed to define the role of allergy and infection in causing nasal inflammation in Aboriginal children with chronic middle ear disease. METHODOLOGY: Thirty-one Aboriginal children aged between 3 and 7 years underwent clinical assessment, audiometry and allergy skin tests. Nasal swabs for bacterial culture and cytology were performed during the winter and again in spring to identify any seasonal variation. A randomized trial of nasal beclomethasone for 8 weeks was conducted in children with abnormal tympanometry to identify the effect of therapy upon nasal cytology. RESULTS: Twenty-six of the 31 children had abnormal tympanograms. Average hearing levels were reduced in nine children. Pathogenic organisms were isolated from most children: Streptococcus pneumoniae (82%), Haemophilus influenzae (79%), Moraxella catarrhalis (39%) and Staphylococcus aureus (29%). Eight of the 31 children (26%) were atopic. Nasal cytology disclosed a marked neutrophil infiltrate (80% of cells) during the winter, which fell significantly in spring to 52% of cells. Only two subjects had nasal eosinophilia of >10%. There was no effect of beclomethasone on nasal cytology. CONCLUSIONS: Chronic ear disease in Aboriginal children is associated with nasal inflammation, neutrophil infiltration and the presence of bacteria. These features suggest respiratory infection as the main cause of chronic nasal inflammation in Aboriginal children with middle ear disease. There is a seasonal variation in the severity of the nasal infiltrate, consistent with increased infections during winter. Despite a high prevalence of atopy, allergic nasal disease was uncommon.

Anti-Inflammatory Agents

The prediction of hospital admission in children with acute asthma.

OBJECTIVE: To determine whether a single assessment of children at the time of presentation to the emergency department would discriminate accurately between those requiring admission and those who could be managed at home and to examine the appropriateness of these decisions. METHODOLOGY: Fifty-three children were assessed using a table recommended by Australian and New Zealand respiratory paediatricians, which categorizes children as probably being able to manage at home (group 1), may need admission to hospital (group 2) and certainly need admission to hospital (group 3) on the basis of oximetry, presence of wheeze and pulsus paradoxus. RESULTS: Nine out of 11 children assigned to group 1 were managed at home and 15/17 who were predicted to require admission were admitted. No individual component of the assessment dominated the decision made. Of the 25 children allocated to group 2, 18 were admitted. CONCLUSIONS: The method employed was highly predictive of outcome for half of the children who presented with asthma. However, 25/53 (47%) were assigned by the table to a recommendation for further assessment; this limits its usefulness.

Acute Disease

Development of bronchial hyperreactivity following transient absence of salivary IgA.

In a birth cohort of 114 normal children, this study examined the hypothesis that a transient absence of salivary IgA in the first year of life was associated with an increased risk of developing atopy, asthma, or bronchial hyperreactivity (BHR) later in life. Episodes of transient absence of IgA in saliva, of less than 1 mo, occurred in 18% of the study population in the first year of life. The children were assessed at age 7.5 to 12 yr for the presence of atopy (skin prick test to inhaled allergens), asthma (wheeze in the previous 12 mo), and BHR (histamine provocation). The transient absence of salivary IgA in the first year of life was associated with an increased risk of BHR (adjusted odds ratio [Adj OR]: 11.6; 95% confidence interval [CI]: 2.2 to 60.9) and a trend toward a lowered risk of atopy to inhaled allergens (raw OR: 0.35; CI: 0.11 to 1.11). There was no relationship between the transient absence of salivary IgA and a clinical diagnosis of asthma (Adj OR: 0.9; CI: 0.2 to 3.6). The inconsistency in the relationships between the transient absence of salivary IgA and atopy, asthma, and BHR supports the concept that atopy, wheeze, and bronchial hyperreactivity are independent clinical outcomes. One possible explanation for the relationships observed in this study is that the transient absence of IgA in saliva in the first year of life identifies a cohort with mucosal hypoimmunity. These subjects are thus less likely to develop atopy and less able to effectively respond to a mucosal infection. Presentation of a mucosal antigen in these subjects may subsequently be associated with an inappropriate inflammatory response, which conditions bronchial hyperreactivity, and which is independent of atopy.

Air Pollutants

Eosinophil apoptosis and the resolution of airway inflammation in asthma.

Asthma is accompanied by the accumulation of potentially damaging eosinophils within inflamed airways. How eosinophils may be removed from the airways is not clear. The phagocytic removal of eosinophils in vitro requires that they undergo apoptosis, a form of cell death. We postulated that eosinophil apoptosis may occur in vivo, promoting the removal of airway eosinophils and the resolution of inflammation in asthma. We examined eosinophil apoptosis in sputum samples obtained from 11 subjects during an asthma exacerbation and 2 wk after corticosteroid treatment of the exacerbation. Airway function improved following corticosteroid treatment, and eosinophilic inflammation subsided, with significant decreases occurring in the number of airway eosinophils and the percentage of activated eosinophils. The proportion of apoptotic airway eosinophils increased significantly following corticosteroid treatment, and eosinophil products were apparent within macrophages. Our findings indicate that eosinophil apoptosis is clinically relevant in asthma. Apoptosis may represent a mechanism that promotes the resolution of eosinophilic inflammation in asthma.

Adrenal Cortex Hormones

Assessment of airway inflammation in children with acute asthma using induced sputum.

The aims of this study were: to assess the safety of a sputum induction method using inhaled normal saline in children with acute asthma; and to investigate changes in sputum cell counts between acute exacerbations of asthma and its resolution. Ultrasonically nebulized normal saline was used to induce sputum from children (n = 8) presenting with acute asthma within 1 h of arrival and again at least 14 days later, after resolution of the exacerbation. Children received pretreatment with bronchodilator, and peak expiratory flow (PEF) was monitored throughout the procedure. Samples were analysed for total cell count, differential cell counts, and for eosinophils and neutrophils using specific immunochemical stains. Sputum induction was performed without adverse effect in each child with acute asthma. The mean fall in PEF from baseline during sputum induction was 5.3% during the acute attack and 3.4% at resolution. A shorter nebulization time was required to induce sputum in acute asthma than at follow-up (7.8 vs 13.9 min; p = 0.04). During acute asthma, there was an intense cellular infiltrate (mean total cell count 34 x 10(6) cells.mL-1), which resolved after recovery (1.9 x 10(6) cells.mL-1) (p = 0.04). The infiltrate was heterogenous, comprising eosinophils (6.7 x 10(6) cells.mL-1), neutrophils (5.4 x 10(6) cells.mL-1) and mast cells (0.47 x 10(6) cells.mL-1). Resolution of the exacerbation was accompanied by a significant fall in eosinophils and neutrophils (p < or = 0.04). Normal saline induction of sputum can be used to assess airway inflammation in acute asthma. Children with acute asthma have intense airway inflammation that is heterogeneous and involves neutrophils, eosinophils and mast cells.

Acute Disease

The use of continuous quality improvement methods to implement practice guidelines in asthma.

National asthma management guidelines have improved awareness of the rising morbidity and mortality from asthma but have not been widely implemented at a local level. This paper describes the use of continuous quality improvement techniques to facilitate the implementation of asthma management guidelines within a tertiary hospital setting. A baseline audit demonstrated satisfactory emergency assessment and treatment, but identified poor compliance with the patient education aspects of the asthma management plan. An evaluation of the literature demonstrated that programs combining asthma education and management were effective when directed towards adults with a recent severe asthma exacerbation. An asthma education and management service was developed to address these deficits. A repeat audit was conducted which identified improvements in asthma control and management skills for patients attending the education program, together with reductions in asthma re-admission rates for patients referred to the service. Ongoing quality assessments will target non-attenders to the service and the maintenance of asthma skills. An area Asthma Health Outcomes Council was formed to address the issues of asthma management throughout the area health service.

Adult

Using quality-control analysis of peak expiratory flow recordings to guide therapy for asthma.

OBJECTIVE: To compare the action points in published asthma management plans with those derived from quality-control analysis of peak expiratory flow recordings. DESIGN: Longitudinal observational study. SETTING: An ambulatory asthma education and management program in a tertiary care hospital. PATIENTS: 35 adults with asthma and exacerbation of asthma. MEASUREMENTS: Peak expiratory flow diaries and symptom recordings. RESULTS: Asthma action points from published asthma management guidelines had poor operating characteristics. The success rate was 35% when the action point was a peak expiratory flow rate less than 60% of the patient's best peak flow. The success rate improved to 88% when the action point was a peak expiratory flow rate less than 80% of the patient's best peak flow. Published action points had a high failure rate. Peak flow decreased to below the published action points during a stable period of asthma in 7% to 51% of patients studied. Action points defined using quality-control analysis did significantly better. A peak flow value less than 3 standard deviations below the patient's mean peak flow detected 84% of exacerbations and had a low failure rate (19%). Other quality-control tests had sensitivities of 91% and 71%. Quality-control action points could detect exacerbations up to 4.5 days earlier than conventional methods. CONCLUSIONS: Individualized action points can be derived for patients with asthma by applying quality-control analysis to peak flow recordings. These action points are more sensitive in detecting exacerbations of asthma and have fewer false-positive results. Action plans developed in this manner should be more useful for the early detection of deteriorating asthma.

Adrenal Cortex Hormones